The results support the idea that a non-1alpha-hydroxylated vitamin D analogue may elicit vitamin D receptor (VDR) effects in 1alpha-hydroxylase expressing parathyroid tumour cells.
A number of genes, put forth as candidate tumor suppressors based on their genomic locations, roles in familial disease, and/or other relevant biological functions, have been examined for pathogenetic mutations in sporadic parathyroid tumors with negative results; these include the calcium-sensing receptor protein (CaR), vitamin-D receptor (VDR), and RET.
Therefore, to assess VDR gene inactivation's potential pathogenetic role in this disease, we rigorously analyzed the VDR gene in 59 parathyroid tumors surgically resected from uremic patients.